Fast carbs are foods that quickly turn into glucose in the body, often before you even finish swallowing. They include sugar, of course, which is half glucose, but the main culprit in the Western diet is wheat flour, which is mostly amylopectin A, the type of starch that is most quickly digested into glucose by the enzymes in your saliva. Making the digestion much faster is the fact that the flour is ground extremely fine, providing enormous amounts of surface that is then exposed to the enzymes.
We have long had a nickname for the effects of fast carbs on the brain: food coma. While the name is meant to be somewhat tongue-in-cheek, the effect is real, as a recent study in the journal Physiology & Behavior shows.
The researchers tested the effects of glucose on simple reaction time, arithmetic, and an effect called Stroop interference, where, for example, printing the word “blue” in a color other than blue slows down thinking. In all three tests, subjects responded more slowly when given glucose or sucrose than when given the sucralose placebo. The effect was greater after a 10 hour fast (such as usually occurs just before breakfast).
The effect after fasting was a 15% slowdown in reaction time. Without fasting, the reaction time was faster, but the difference between glucose and placebo was greater, with glucose causing a 17% slowdown.
Other studies have shown that glucose induces sleep by activating sleep-promoting neurons in the brain, and that by raising insulin levels, glucose can make it easier for the amino acid tryptophan to enter the brain, where it is converted into the hormones serotonin and melatonin, both of which are involved in sleep. The tryptophan you get from that Thanksgiving turkey would not by itself make you sleepy. It is the insulin following the rolls, mashed potatoes, and desserts that allows it to get into the brain.
A study in the journal Nature confirms that bad gut microbes are involved in the causes and progress of Non-Alcoholic Fatty Liver Disease (NAFLD), a dangerous complication of obesity. The same diet that causes obesity causes disruptions in the normal healthy ecology of microbes in the human gut, causing pathogenic bacteria to proliferate. These harmful bacteria have been linked to NAFLD, but now the mechanisms of the disease are becoming clear.
The harmful bacteria produce molecules called endotoxins. These are actually structural parts of the bacterial wall, made of carbohydrate and fat. These toxins enter the bloodstream and are sent to the liver, where they cause inflammation.
Chronic inflammation is the cause of many different problems in the body, such as diabetes, Alzheimer’s Disease, arthritis, atherosclerosis, heart disease, and stroke. Obesity itself also causes chronic inflammation, because fatty tissue is one of the places where inflammatory immune cells live, and having dangerous amounts of fatty tissue throws the immune system towards being always on, as if we were fighting an infection.
In the case of gut dysbiosis (the accumulation of harmful gut microbes), we actually are fighting an infection. By changing the diet towards one of lower carbohydrate and fat, and much higher fiber along with protein, we can feed the good bacteria in the gut at the expense of the bad bacteria, and restore a healthy balance. Not only will this reduce the likelihood of fatty liver disease, but it will also reduce fatty tissue, and the inflammation it causes.
As a further benefit, healthy gut bacteria can actually help you keep the weight off. Dysbiosis is both a contributing cause and an effect of obesity, in a kind of vicious cycle. Getting rid of one helps to get rid of the other. When you reach for a snack, try an apple or a carrot instead of the cookies or cupcake. Your gut will thank you for it.
Obesity is a cancer risk that rivals smoking as a preventable leading risk factor for cancer death. While cancer is assisted by the hyper-nutrition, gut microbe disturbance, cholesterol, and diabetes that accompany obesity, it is particularly aided by the fifth consequence of being overweight: chronic inflammation.
Chronic inflammation increases cancer risk both in the initiation of the disease, and the progression of the disease, by cultivating an environment that encourages the mutations in cells that lead to cancer. The changes inflammation brings to tissues make them better places for malignant cells to live and grow.
Fat is not just an energy storage tissue. It is also where many inflammatory immune cells live. The more fat we have, the more immune cells there are, pouring out inflammatory molecules that change tissues and increase cancer risk.
A recent study in the journal Science shows that some cancers are actually addicted to obesity, requiring the hyper-nutrition and inflammatory molecules to survive. Breast cancer is promoted by blood vessel growth factors produced by fat cells. Pancreatic cancer is associated with interleukin-1-beta, a immune system suppressor molecule produced by fat cells. Fat cells secrete molecules that allow prostate cancer cells to invade surrounding tissue.
Fat cells also produce estrogen, which can make estrogen sensitive cancers grow faster. They also produces insulin and other growth factors that affect all tissues.
Screening for breast cancer is hindered by surrounding fatty tissue, but worse than that, fat cells produce growth factors that promote metastasis (the spreading of cancer to other tissues such as the lungs). High cholesterol levels associated with obesity also cause breast cancer cells to metastasize. Metastasis is what causes most breast cancer deaths.
Losing weight can help to prevent cancer, and can help prevent existing cancer from spreading. Fasting reduces immune suppression, helping the immune system fight off cancer. Exercise activates natural killer cells in the immune system that seek out and destroy cancer cells.